Hypoxia-induced reactive oxygen species in organ and tissue fibrosis

被引:0
作者
Xie, Linshen [1 ,2 ]
Wang, Qiaolan [1 ,2 ]
Ma, Jingxuan [1 ,2 ]
Zeng, Ye [3 ]
机构
[1] Sichuan Univ, West China Sch Publ Hlth, Chengdu 610041, Peoples R China
[2] Sichuan Univ, West China Hosp 4, Chengdu 610041, Peoples R China
[3] Sichuan Univ, Inst Biomed Engn, West China Sch Basic Med Sci & Forens Med, Chengdu 610041, Peoples R China
关键词
Fibrosis; Oxidative stress; Hypoxia; MESENCHYMAL STEM-CELLS; OXIDATIVE STRESS; INDUCIBLE FACTOR-1-ALPHA; PULMONARY-FIBROSIS; REPERFUSION INJURY; RENAL FIBROSIS; EXPRESSION; ACTIVATION; HIF-1-ALPHA; ACCUMULATION;
D O I
暂无
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Fibrosis is the end-stage change of damaged tissues in various human diseases, which can lead to permanent scarring or organ malfunction. Hypoxia leads to oxidative stress, mitochondrial dysfunction, and inflammation in dysfunctional organs and tissues. Oxidative stress resulting from the overproduction of reactive oxygen species plays a central role in the fibrosis of injured organs. This review addresses the updated knowledge of the relationship between hypoxia and tissue fibrosis mediated by the reactive oxygen species pathway. Moreover, novel anti -fibrotic strategies are discussed, which may suppress reactive oxygen species and organ fibrosis.
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收藏
页码:261 / 267
页数:7
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